Abstract
The immunogenicity of a herpesvirus hominis type‐2‐transformed hamster cell line (HSV‐2–333–2–26) of low spontaneous metastatic ability was compared with that of its two in vivo‐derived sublines of increased metastatic potential. The parent (HSV‐2–333–2–26) tumour was immunogenic as assessed by protection against tumour challenge afforded by implantation of irradiated tumour cells or tissue. In contrast, the two metastatic sublines, designated Met A and Met B, were non‐immunogenic as defined by the above critera. However, the parent Met A and Met B tumours were shown to possess a common antigen(s), since immunization with irradiated parent tumour cells afforded protection to challenge with Met A or Met B. Immunization with the metastatic sublines, however, gave no protection to homologous or heterologous tumour challenge. Bacillus Calmette‐Guérin (BCG) inoculated in admixture with irradiated tumour cells and followed 7 days later by one immunization with X‐irradiated tumour cells alone, increased host immunocompetence to subsequent homologous or cross‐tumour cell challenge with parent, Met A or Met B cells. The immunity raised by using BCG plus irradiated tumour cells was shown to be specific to antigens expressed on the HSV‐2 parent cell line and its metastatic sublines. In addition, BCG admixed with live inocula of parent, Met A or Met B cells induced contact suppression of in vivo tumour growth of the parent cells, but not of Met A or Met B cells. It is suggested from these studies that the parent tumour possesses a tumour‐specific transplantation antigen(s)(TSTAs) which is not functionally active on its metastatically derived sublines. Common antigens, shared between the parent and Met A and Met B cells, are detectable by cross‐challenge experiments, but they themselves appear not to be immunologically offensive. The loss of immunogenicity is discussed as a possible mechanism for the in vivo selection of sublines with increased metastatic potential.